MicroRNA-19b-1 reverses ischaemia-induced heart failure by inhibiting cardiomyocyte apoptosis and targeting Bcl2 l11/BIM

Ischaemia induces cardiac apoptosis and leads to a loss of cardiac function and heart failure after myocardial infarction. MicroRNA-19b-1 (miR-19b-1), a key member of the miR-17/92 cluster, plays crucial roles in inhibiting apoptosis. However, the role of miR-19b-1 in ischaemia-induced heart failure...

Full description

Saved in:
Bibliographic Details
Published in:Heart and vessels 2019-07, Vol.34 (7), p.1221-1229
Main Authors: Yang, Wenbo, Han, Yanxin, Yang, Chendie, Chen, Yanjia, Zhao, Weilin, Su, Xiuxiu, Yang, Ke, Jin, Wei
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Bcl-2 protein
Bcl-2-Like Protein 11 - genetics
BIM protein
Biomedical Engineering and Bioengineering
Cardiac Surgery
Cardiology
Cardiomyocytes
Cell Proliferation - genetics
Cells, Cultured
Congestive heart failure
Disease Models, Animal
Down-Regulation
Gene expression
Heart
Heart attacks
Heart failure
Heart Failure - pathology
Heart Failure - therapy
Human Umbilical Vein Endothelial Cells
Humans
Ischemia
Macrophages
Medicine
Medicine & Public Health
Mice
Mice, Inbred C57BL
MicroRNAs
MicroRNAs - administration & dosage
MicroRNAs - genetics
MicroRNAs - metabolism
miRNA
mRNA
Myocardial infarction
Myocardial Infarction - etiology
Myocardial Infarction - pathology
Myocardial Infarction - therapy
Myocytes, Cardiac - physiology
Original Article
Ribonucleic acid
RNA
Vascular Surgery
Ventricle
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Ischaemia induces cardiac apoptosis and leads to a loss of cardiac function and heart failure after myocardial infarction. MicroRNA-19b-1 (miR-19b-1), a key member of the miR-17/92 cluster, plays crucial roles in inhibiting apoptosis. However, the role of miR-19b-1 in ischaemia-induced heart failure remains unknown. In this study, ischaemia resulted in cardiac apoptosis and the suppression of miR-19b-1 expression, whereas miR-19b-1 overexpression inhibited ischaemia-induced cardiac apoptosis in vivo and in vitro. Moreover, miR-19b-1 not only attenuated the infarct size but also ameliorated heart failure after myocardial infarction, including the changes in the left ventricular ejection fraction and volume load. Mechanically, miR-19-1 targeted and downregulated the mRNA and protein expression of Bcl2l11/BIM, a pro-apoptotic gene of the Bcl-2 family. Together, these results revealed an essential role of miR-19b-1 in ischaemia-induced heart failure.
ISSN:0910-8327
1615-2573
DOI:10.1007/s00380-018-01336-3